Dietary sodium intake can have a profound influence on blood pressure of hypertensive patients. Kempner demonstrated many years ago that reduction of dietary sodium could control high blood pressure and even reverse end-organ damage of patients with severe and malignant hypertension. However, the mechanism of blood pressure regulation by dietary sodium has never been established. We have recently found that renal Alpha (2)-receptor desnity even more. We are proposing studies on the functional role of renal Alpha (2)-adrenergic receptors and to question the hypothesis that this abnormality might be involved in a hypertensive mechanism. Genetic studies are proposed which will determine some of the characteristics of inheritance of this biochemical abnormality and hopefully tell us whether the abnormality is causing the high blood pressure, and if so, to what extent. Interestingly, the renal Alpha (2)-receptor may be the first example of initially demonstrating a receptor biochemically followed by the search for a functional and possibly phatogenetically linked to hypertension, this biochemical abnormality may provide new approaches to clinical and basic research in hypertension and a rationale for controlling dietary sodium of selected individuals in our population.